An animal model of Candida albicans endocarditis has been established in rabbits. In previous work we have characterized the disease, determined the efficacy of therapy, quantitated the antibody response of infected rabbits and described why the host fails to eradicate the fungus from the heart valve. The latter study indicated that the fungus prefers the traumatized endocardium of the heart valve for colonization. Therefore, we will determine what component(s) of the host and/or fungus are responsible for the early adherence of the fungus to the endocardium by using a fibrin tissue culture system. Other preliminary studies with a bacterial endocarditis model have indicated that pre-immunization of animals affords some degree of protection against endocarditis. We would like to further investigate this aspect by immunizing rabbits with C. albicans and comparing the LD50 of preimmunized rabbits to non-immunized rabbits. Within 5-6 days following infection, the vegetation which has formed on the heart valve is composed almost entirely of fungal elements. Host components are seldom observed. Therefore, I will also characterize, using an invitro system, the degradative extracellular enzymes of C. albicans and the substrates in heart valve connective tissue which they act upon. Finally, I hope to develop a precipitin or agglutination test which will detect specifically antibody from rabbits with endocarditis, i.e., endocarditis-specific antibody. This will be accomplished by purifying components from a cytoplasmic extract of C. albicans and testing them for their ability to react with sera from rabbits with endocarditis but not with sera from i.v.-infected rabbits without endocarditis. Another approach to the detection of the disease is to find fungal antigens in the sera of infected animals. This will be accomplished using a hemagglutination inhibition assay.